p75TNFR激活型单克隆抗体对脑创伤小鼠炎症反应的保护作用

Effect of p75TNFR monoclonal antibody on the inflammation in brain trauma mice

目的通过单克隆抗体激活p75TNFR信号通路，观察对小鼠脑创伤后关键炎症信号转导通路p38MAPK活化水平和炎症因子表达水平的影响，并探讨其作用机制。方法参照Feeney等的自由落体法制作小鼠创伤性颅脑损伤模型，运用Western-blot方法检测炎症信号通路中关键分子p38MAPK变化，采用ELISA方法检测注射了D8F2的小鼠血清中炎症因子IL-6、TNF-α和IL-β水平的变化。结果创伤后TNF—α、IL-1β、IL-6水平均明显升高，治疗组则低于创伤组，且更快恢复至正常水平。创伤后体内p38MAPK迅速激活至较高水平，治疗组则低于创伤组，且下降更快。结论在小鼠脑创伤模型中D8F2能通过抑制p38MAPK活化，抑制炎症因子水平的升高，对脑创伤小鼠炎症损害起保护作用。

Objective To observe the activation level of key p38MAPK in inflammation signaling pathways, and the expression level of inflammatory cytokines in the brain traumatic mice and to explore the mechanisms by signaling pathways of the p75TNFR monoelonal antibody. Methods According to the method of free fall such as Feeney, traumatic head injury was made in mice model, the changes of key p38MAPK in inflammation signaling pathways were observed by Western - blot, and the changes of serum inflammation factors including IL - 6, TNF - α and IL - 1β level in the mice with the injection of p75TNFR monoclonal antibody were detected by ELISA. Results TNF - α, IL - 1β, IL - 6 level increased obviously after brain trauma, those in the treatment group was lower compared with traumatic group, and returned to normal levels fast. p38MAPK was activated quickly to the higher level after brain trauma, p38MAPK in the treatment group was lower compared with traumatic group, and decreased fast. Conclusion In the little mice models of brain trauma, D8F2 can inhibit the activation of p38MAPK, limit the increase of inflammatory cytokines level, and protect the brain trauma mice from inflammatory injury.